Role of the renal sympathetic nerve activity in determining salt sensitivity.

盐依赖性高血压的潜在机制尚不完全清楚。肾交感神经活动（RSNA）对肾血流量、肾素释放和尿钠排泄的控制有直接影响。1.我们记录了自由活动的Dahl盐敏感（DS）和盐抵抗（DR）大鼠在低NaCl饮食下的RSNA。(1)在静息状态下，观察到两种类型的放电模式，分组心脏相关放电（GD）和非分组不规则放电（NGD）。静脉注射苯乙酰氯可抑制GD，而对NGD无抑制作用。在DS和DR大鼠中均观察到GD和NGD，并且通过静脉注射神经节阻滞剂氯化六甲双铵完全消除。(2)在Dahl-R和Dahl-S大鼠中，与静息水平相比，高渗NaCl溶液的l. c. v.输注显著增加动脉血压并降低RSNA。然而，RSNA对NaCl的反应性在两组中没有差异。心率没有显著变化。(3)在0.3M NaCl灌注期间，Dahl-S大鼠的水摄入量与Dahl-R大鼠相比减少。2.接下来，使用清醒的Sprague-Dawley大鼠，我们检测了RSNA对中枢盐负荷的反应性。静脉注射高渗氯化钠溶液后，RSNA的抑制反应：（1）在戊巴比妥麻醉下，RSNA的抑制反应大大减弱。(2)在清醒的大鼠不接触水的情况下增强。(3)在去窦弓神经（SAD）清醒大鼠中观察到。(4)血管加压素V_1拮抗剂（OPC-21268，i. v.）而V_2拮抗剂（OCP-31260）则无此作用。

The mechanisms underlying salt-dependent hypertension are not entirely known. Renal sympathetic nerve activity (RSNA) has a direct effect on the control of renal blood flow, renin release and urinary sodium excretion.1.We have recorded RSNA in free-moving Dahl salt sensitive (DS) and salt-resistant (DR)-rats on a low NaCl diet.(1) Under resting conditions, two types of discharge patterns were seen, a grouped cardiac-related discharge (GD) and a non-grouped irregular discharge (NGD). The GD was inhibited by i.v.administration of phenylephrine chloride, while the NGD was not. Both GD and NGD were seen in DS and DR rats and both were completely abolished by i.v.administration of the ganglionic blocker, hexamethonium chloride.(2) l.c.v.infusion of hypertonic NaCl solution significantly increased arterial blood pressure and decreased RSNA compared with the resting levels in both Dahl-R and Dahl-S rats. However, the responsiveness of RSNA to NaCl did not differ in either group. Heart rate did not significantly change.(3) During 0.3 M NaCl infusion, water intake in Dahl-S rats was diminished compared with that in Dahl-R-rats.2.Next, using conscious Sprague-Dawley rats, we have examined responsiveness of RSNA in response to central salt loading. The inhibitory response of RSNA following i.c.v.administration of hypertonic NaCl solution were,(1) greatly attenuated under pentobarbital anesthesia.(2) enhanced in conscious rats not access to water.(3) observed in sinoaortic denervated (SAD) conscious rats.(4) significantly attenuated by pretreatment with vasopressin V_1 antagonist (OPC-21268, i.v.) but not V_2 antagonist (OCP-31260).